Nasopharyngeal carcinoma (NPC) is a malignant epithelial carcinoma of the head and neck region which mainly distributes in southern China and Southeast Asia and has a crucial association with the Epstein–Barr virus. Based on epidemiological data, both incidence and mortality of NPC have significantly declined in recent decades grounded on the improvement of living standard and medical level in an endemic region, in particular, with the clinical use of individualized chemotherapy and intensity-modulated radiotherapy (IMRT) which profoundly contributes to the cure rate of NPC patients. To tackle the challenges including local recurrence and distant metastasis in the current NPC treatment, we discussed the implication of using targeted therapy against critical molecules in various signal pathways, and how they synergize with chemoradiotherapy in the NPC treatment. Combination treatment including targeted therapy and IMRT or concurrent chemoradiotherapy is presumably to be future options, which may reduce radiation or chemotherapy toxicities and open new avenues for the improvement of the expected functional outcome for patients with advanced NPC.

As a key member of the forkhead box transcription factors, forkhead box F2 (FOXF2) serves as a transcriptional regulator and regulates downstream gene expression in embryonic development, metabolism and in some common diseases, such as stroke and gastroparesis. Recent studies have shown that aberrant expression of FOXF2 is associated with a variety of tumorigenic processes, such as proliferation, invasion and metastasis. The role of FOXF2 in the development of many different organs has been confirmed by studies and has been speculated about in case reports. We focus on the mechanisms and signal pathways of tumour development initiated by aberrant expression of FOXF2, and we summarize the diseases and signal pathways caused by aberrant expression of FOXF2 in embryogenesis. This article highlights the differences in the role of FOXF2 in different tumours and demonstrates that multiple factors can regulate FOXF2 levels. In addition, FOXF2 is considered a biomarker for the diagnosis or prognosis of various tumours. Therefore, regulating the level of FOXF2 is an ideal treatment for tumours. FOXF2 could also affect the expression of some organ-specific genes to modulate organogenesis and could serve as a biomarker for specific differentiated cells. Finally, we present prospects for the continued research focus of FOXF2. Facts FOXF2 exhibits inhibitory effects in most tumours. In lung cancer (except for non-small cell lung cancer) and rhabdomyosarcoma in mice, FOXF2 mainly shows a promotive effect. FOXF2 can both inhibit and promote HCC and breast cancer. Regulating the expression level of FOXF2 is an ideal treatment for tumours. Mutations in or deletions of FOXF2 occur in some patients with craniofacial deformities. Mice with suppressed FOXF2 expression show defective organogenesis, such as aglossia, eye deformity, cleft palate and intracranial haemorrhage. Open questions Does FOXF2 have a common mechanism in tumours? What signalling pathways and gene expression does FOXF2 affect in the development of different organs? Are there any specific mechanisms or proteins that can be targeted in the treatment of a FOXF2-affected diseases?

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Metastasis is the main cause of death in patients with nasopharyngeal carcinoma (NPC). The molecular mechanisms underlying the metastasis of NPC remain to be elucidated. TBL1X has been shown abnormally expressed in diverse cancers. However, the role and mechanism of TBL1X in NPC remain unknown. Here, we showed TBL1X expression was significantly higher in metastatic NPC tissues compared to non-metastatic tissues and significantly correlated with TNM stage and metastasis of NPC patients. In addition, NPC patients with high TBL1X expression had a poor prognosis. TBL1X interacted with TCF4 to trans-activate Flot2 expression. TBL1X promoted NPC cell migration and invasion in vitro and in vivo through Flot2. Moreover, Flot2 increased the expression of TBL1X by upregulating c-myc, which was identified to be a positively regulatory transcription factor of TBL1X. TBL1X could restore the functional changes of NPC cells resulting from Flot2 alteration. TBL1X and Flot2 were positively correlated in NPC. Patients with high expression of both TBL1X and Flot2 possessed poorer overall survival (OS) and disease-free survival (DFS) compared to patients with high expression of any single one of the two proteins. Our findings demonstrate that TBL1X and Flot2 positively regulate each other to promote NPC metastasis, which provides novel potential molecular targets for NPC treatment.

NADH:ubiquinone oxidoreductase core subunit S8 (NDUFS8) is an essential core subunit and component of the iron-sulfur (FeS) fragment of mitochondrial complex I directly involved in the electron transfer process and energy metabolism. Pathogenic variants of the NDUFS8 are relevant to infantile-onset and severe diseases, including Leigh syndrome, cancer, and diabetes mellitus. With over 1000 nuclear genes potentially causing a mitochondrial disorder, the current diagnostic approach requires targeted molecular analysis, guided by a combination of clinical and biochemical features. Currently, there are only several studies on pathogenic variants of the NDUFS8 in Leigh syndrome, and a lack of literature on its precise mechanism in cancer and diabetes mellitus exists. Therefore, NDUFS8-related diseases should be extensively explored and precisely diagnosed at the molecular level with the application of next-generation sequencing technologies. A more distinct comprehension will be needed to shed light on NDUFS8 and its related diseases for further research. In this review, a comprehensive summary of the current knowledge about NDUFS8 structural function, its pathogenic mutations in Leigh syndrome, as well as its underlying roles in cancer and diabetes mellitus is provided, offering potential pathogenesis, progress, and therapeutic target of different diseases. We also put forward some problems and solutions for the following investigations.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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In order to understand the changes of water quality in the water, the paper uses the improved BP network of LM algorithm to learn and train the data, and implements the neural network model on the MATLAB platform, and uses the processed samples for the established BP neural network. Learning training, in order to prevent some neurons from reaching the state of supersaturation.By normalizing the data, the trained network is used to predict the water quality indicators of the Luanhe River Line. The results show that it is feasible to evaluate the water quality along the sputum by BP neural network model. The model has strong learning, association and fault tolerance functions. The analysis results and process are close to the thinking process and analysis method of the human brain, which makes the water quality evaluation. The accuracy of the results is greatly improved.